EFFECT OF THYROID STATUS IN THE PERINATAL-PERIOD ON OXIDATIVE CAPACITIES AND MITOCHONDRIAL RESPIRATION IN PORCINE LIVER AND SKELETAL-MUSCLE

Citation
P. Herpin et al., EFFECT OF THYROID STATUS IN THE PERINATAL-PERIOD ON OXIDATIVE CAPACITIES AND MITOCHONDRIAL RESPIRATION IN PORCINE LIVER AND SKELETAL-MUSCLE, Reproduction, fertility and development, 8(1), 1996, pp. 147-155
Citations number
33
Categorie Soggetti
Reproductive Biology","Developmental Biology
ISSN journal
10313613
Volume
8
Issue
1
Year of publication
1996
Pages
147 - 155
Database
ISI
SICI code
1031-3613(1996)8:1<147:EOTSIT>2.0.ZU;2-F
Abstract
Regulatory thermogenesis is reduced in newborn piglets which have been made hypothyroid during late gestation by giving the sow a high gluco sinolate rapeseed diet (test animals). Thereafter, the progressive inc rease in thermogenic capacity parallels the development of a marked po stnatal hyperthyroid state. To explain these effects of thyroid hormon es at the tissue and mitochondrial levels, we have examined both liver and skeletal muscle to determine possible underlying changes in (i) t issue oxidative capacities (cytochrome oxidase (GO) activity), between 80 d of gestation and 48 h after birth, and (ii) mitochondrial conten t and respiratory capacities at 24 h of life. In control piglets, CO a ctivity increased sharply during late gestation and the first 2 d of l ife in liver and rhomboideus (RH) muscle (P < 0.01), whereas only a pr enatal increase was observed in longissimus dorsi (LD) muscle. Test fe tuses were hypothyroid and had lower CO activities than controls durin g late gestation in RH muscle (P < 0.06, at 110 d of gestation; P < 0. 08, at birth) and in liver (P < 0.001, at birth). The postnatal increa se in CO activity in RH muscle and liver was higher (P < 0.05) in test than in control piglets, and as a result the difference between the 2 groups was not significant by 24-48 h of life. There was no effect of treatment on LD muscle. At 24 h, hyperthyroid test piglets had lower amounts of mitochondrial proteins than controls (P < 0.05) in all thre e tissues, possibly reflecting reduced mitochondrial protein synthesis during fetal life and suggesting that high postnatal T-3 levels did n ot bring about major increases in protein synthesis within 24 h. Howev er, test piglets exhibited higher rates of mitochondrial respiration t han controls in liver and RH muscle, as shown by increases in State II I and FCCP-stimulated respirations (P < 0.05), and mitochondrial CO an d creatine kinase activities (P < 0.05). In RH muscle, both subsarcole mmal and intermyofibrillar mitochondria showed the same trends. No cha nges were observed in LD muscle. Our results describe for the first ti me the effect of thyroid hormones on perinatal oxidative capacities an d neonatal mitochondrial respiration in liver and skeletal muscle of t he pig, through both the short-term regulation of mitochondrial respir ation and the long-term control of mitochondrial biogenesis. The diffe rential sensitivity of LD and RH muscles to thyroid hormones is discus sed.